I often hesitate to make broad, sweeping claims about the nature, cause, and experience of eating disorders and disordered eating. However, if there is one thing I feel absolutely certain saying about these disorders, it is that they are incredibly complex and multifaceted with no “one-size fits all” solution. So, I was quite excited when I came across a recent article by Michael Strober and Craig Johnson (2012) that explores the complexity of eating disorders and their treatment. Both authors have significant clinical experience treating eating disorders.
This article uses cases studies, literature, and the authors’ collective clinical experience to respond to some of the key controversies surrounding anorexia and its treatment. Among the major controversies that have come to light of late, they focus on two:
The authors’ exploration of these topics supports an overall argument: focusing on singular explanations and solutions for anorexia, particularly through the vehement defense of any particular approach, obscures the complexity of the disorder, as well …
Is anorexia nervosa a subtype of body dysmorphic disorder (BDD)? Well, probably not, but don’t click the close button just yet. In this post, I’ll explore the relationship between anorexia nervosa and BDD, and discuss how understanding this relationship might help us develop better treatments for both disorders.
Despite the fact that there are obvious similarities between the disorders, studies exploring the relationship between BDD and AN are few and far between. In a recent paper, published in the Clinical Psychology Review, Andrea Hartmann and colleagues summarized the current state of knowledge in the field. The review compared clinical, personality, demographic, and treatment outcome features of AN and BDD. I’ll summarize the key points of the paper in this post.
(I will be focusing on the relationship between AN and BDD, as opposed to EDs and BDD, because that’s the scope of the review article.)
First, what is body dysmorphic disorder?
Approximately 1/3 of individuals do NOT recognize that the beliefs about their appearance are due to a mental disorder and 2/3 believe that other people are laughing/staring …
The association between drug abuse and eating disorders (EDs) is not new. Since the 1970s, doctors have reported higher incidents of self-medication and drug abuse in a subset of eating disorder patients. Drugs, in this context, cover everything from laxatives and diet pills, to alcohol and street drugs.
The association between drug use and EDs is not shocking; however, the extent of the problem is likely overlooked.
In a report detailing the most comprehensive review on the topic, the National Center on Addiction and Substance Abuse concluded: “Individuals with eating disorders are up to five times likelier to abuse alcohol or illicit drugs and those who abuses alcohol or illicit drugs are up to 11 times likelier to have eating disorders.”
The report is freely available online and I highly recommend reading the entire document.
Here are some of the MAIN FINDINGS:
EDs and substance abuse share many risk factors and this may explain the high rate of co-occurrence. Risk factors include:
…
When most people think of bulimia nervosa, they think of binge eating and self-induced vomiting. While that is not incorrect, it is not the full picture either. In the current edition of the Diagnostic and Statistical Manual (DSM-IV), there are two subtypes of bulimia nervosa: purging (BN-P) and nonpurging (BN-NP). The difference lies in the types of compensation methods: patients with BN-P engage in self-induced vomiting, or the misuse of laxatives, diuretics, or enemas whereas patients with BN-NP use fasting or excessive exercise to compensate for binge eating.
How common in BN-NP? It is very hard to say. A small population-based study in Finland (less than 3,000 participants) found that 1.7% of the sample that bulimia nervosa, 24% had BN-NP (or 0.4% of the entire sample) (Keski-Rahkonen et al., 2009). (I couldn’t find much else on prevalence of BN-NP.)
Unfortunately, however, there’s been very little research on BN-NP.
So little, in fact, that many have wondered if it make sense to subtype bulimia nervosa patients into purging and nonpurging groups? And are there differences between patients with BN-NP and …
EDIT: I want to apologize for an oversight in this blog entry. Shelly and I forgot to mention Diabulimia Helpline in our list of organizations that help raise awareness and support sufferers with type 1 diabetes and eating disorders. Diabulimia Helpline is the only non-profit in the US dedicated to “education, support, and advocacy for diabetics with eating disorders, and their families.” I also want to highlight some services that Diabulimia Helpline offers: “a 24 hour helpline available via (425) 985-3635, an insurance specialist to walk clients and/or their parents through the complicated world of getting insurance to cover eating disorders, and a referral service to help people find the treatment centers, doctors, therapists, and counselors that would be a good fit for them on their road to recovery.” – Sincerely, Tetyana
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Type 1 diabetes (DMT1, or T1DM) is a lifelong disease often diagnosed in children or adolescents. Though causes of DMT1 are complex and not fully understood, it results from the body’s immune system destroying its own insulin-producing cells. This drastically lowers insulin levels and leads to …
Hello Science of Eating Disorders readers! This is a guest post by Liz. Liz is a PhD Candidate in Psychology at the University of Toronto. You can read more about her research, interests, and eating disorder history on her “About” page.
And the usual “disclaimer”: Please keep in mind that I (Tetyana) give as much freedom as possible to guest writers and contributors to write about their own interests and viewpoints. That means that we don’t all necessary agree; there is no joint agenda. My primary reason for wanting more contributors is to widen the content, vary the writing styles, and negate the individual biases we all have. Our desire to understand, translate, and summarize peer-reviewed ED literature is what we all share in common.
Also, the Science of Eating Disorders blog is now one years old! My first post was published on April 3rd, 2012. Thank you everyone for reading, sharing, and commenting. Science blogging is a blast! I’ve learned a lot about eating disorders and science communication! Cheers! – Tetyana
The recent New York City …
The first published case of a late-onset eating disorder (at the age of 40) was in 1930 by John M. Berkman. In 1936, John A. Ryle published a case study of an eating disorder in a 59-year-old woman. Just how common are eating disorders in late middle-age or elderly individuals?
There aren’t a lot of studies on this topic, but the the above figures illustrate that there’s a significant minority of elderly individuals who struggle with eating disorders or disordered eating.
What causes or precipitates eating disorders in late adulthood? Well first, it is important to keep in mind that a proportion of eating disorders in late-life occur in women who either never recovered from their early onset eating disorder or in those who had a remitting/relapsing ED pattern throughout life. But many do develop eating disorders for the first time in their 50′s, 60′s, and 70′s.
In 2010, Maria Lapid and colleagues published a review paper of all the published case studies of eating disorders in individuals over the age of 50. They found 48 studies. I’ve summarized the …
In my last post I talked about some methods that scientists use to study the genetics of eating disorders. I focused on a subfield of genetics called behavioural genetics (which you can think of as a field that attempts to understand, in part, the interplay of genetics and environment in behaviour). In this post I’ll shift gears and focus on molecular genetics. I’ll be working of the same review paper by Drs. Zerwas and Bulik (2011). Molecular geneticists study the structure and function of genes on a molecular level. For example, they try to understand how different mutations or alterations in the genetic code can affect protein function and lead to disease states.
Genetic association studies are hypothesis driven. This means that researchers make a list of genes that are known to be involved in biological mechanisms or behaviours that are affected in eating disorders, such as appetite, mood regulation, reward, anxiety, weight regulation, and so on. Then, they compare these genes in eating disorder patients and in healthy controls to try to identify any differences between the two …
Today I thought I’d take the time to do an overview of what researchers know about the genetics of eating disorders and try to clear up some common misconceptions. The bulk of the content in this blog post comes from a very nice review paper published in 2011 by Drs. Stephanie Zerwas and Cynthia Bulik on the genetics and epigenetics of eating disorders. In an effort to keep blog posts short, this will be a multi-part mini-series.
When it comes to the genetics of eating disorders, there are two main questions that research ask: What is the relative contribution of genetic factors to eating disorder behaviours? And what are those genetic factors? I’ll talk about research attempting to answer the first question in this post and the second question in my next post.
In order to understand the role that genetics plays in influencing eating disorder behaviours, researchers use family, twin, and to a lesser extent, adoption studies.
In family studies, researchers are typically asking What is the probability that a relative of someone with an eating disorder will also …
Avoiding Refeeding Syndrome in Anorexia Nervosa
Refeeding syndrome (RS) is a rare but potentially fatal condition that can occur during refeeding of severely malnourished individuals (such as anorexia nervosa patients). After prolonged starvation, the body begins to use fat and protein to produce energy because there are not enough carbohydrates. Upon refeeding, there’s a surge of insulin (because of the ingested carbohydrates) and a sudden shift from fat to carbohydrate metabolism. This sudden shift can lead to a whole set of problems that characterize the refeeding syndrome.
For example, one of the key features of RS is hypophosphotemia: abnormally low levels of phosphate in the blood. This occurs primarily because the insulin surge during food ingestion leads to a cellular uptake of phosphate. Phosphate is a very important molecule and its dysregulation affects almost every system in the body and can lead to ”rhabdomyolysis, leucocyte dysfunction, respiratory failure, cardiac failure, hypotension, arrhythmias, seizures, coma, and sudden death.”
I’m not, however, going to go into too much detail on RS as there are pretty good sources available here, here, and here. Instead, I want …